systems failure: heart failure

Question 1

renin/angiotensin/ aldosterone system

Answer 1

• regulating blood vol, arterial BP, cardiac and vascular function.
• most important sire for renin release is the kidney.
• sympathetic stimulation (via b-adrenoreceptors), renal artery hypotension, and decreased sodium delivery to the distal tubules stimulate release of renin by the kidney from the juxtaglomerular apparatus (JGA).
• renin is an enzyme that acts upon a circulating substrate, angiotensinogen, that undergoes proteolytic cleavage to form the decapeptide angiotensin I.
• vascular endothelium, particularly in lungs, has an enzyme, angiotensin converting enzyme ACE, that cleaves off two amino acids to form the octapeptide, angiotensin II (AII)

Question 2

angiotensin II

Answer 2

• constricts resistance vessels (via AII receptors) thereby increasing systemic vascular resistance and arterial pressure
• acts upon the adrenal cortex to release aldosterone, which acts upon the kidneys to increase sodium and fluid retention, increasing blood vol
• stimulates release of antidiuretic hormone ADH which acts upon the kidneys to increase fluid retention
• stimulates thirst
• stimulates hypertrophy of cardiac muscle and arterial smooth muscle

Question 3

backward heart failure

Answer 3

fluid congestion

Question 4

forward heart failure

Answer 4

inadequate blood flow to tissues

Question 5

acute heart failure

Answer 5

events take place rapidly and consequence is forward failure (shock)

Question 6

chronic heart failure

Answer 6

compensatory mechanisms may be brought into play and backward failure dominates (congestion)

Question 7

compensatory mechanisms

Answer 7

once LV dysfunction occurs, a series of compensatory mechanisms are triggered:
muscle mass increases- allowing heart to eject more blood, but requires more oxygen to oxygenate the increased muscle mass.
ventricular chamber enlargement- increases amount of blood in ventricle, so ejects more (Frank-Starling Law), but at cost of fluid retention.
sympathetic stimulation- increased heart rate, contractility, redistribution and retention of fluid.
- leading to a host of structural and neurohormonal adaptations

Question 8

cardiac remodelling

Answer 8

• hypertrophy in response to increased demands
• adrenergic stimuli, cytokines (TNFa), and Angiotensin II mediate effects
• beneficial in increasing cardiac output
• these stimuli also have adverse effects

Question 9

causes of LVF

Answer 9

• ischaemic heart disease
• longstanding hypertension
• valve disease (aortic and mitral)
• cardiomyopathies
• congenital heart disease

Question 10

liver congestion

Answer 10

‘nutmeg liver’- speckled appearance of cut liver in chronic venous congestion, due to dilated and congested red central veins surrounded by a paler, unaffected liver tissue.
most frequently seen in RHF

Question 11

congestive cardiac failure

Answer 11

a combination of both left and right ventricular failure

- commonest cause is ischaemic disease followed by other causes of LVF

Question 12

high output cardiac failure

Answer 12

heart muscle essentially normal but output cannot adequately perfuse tissue.

• arteriovenous fistula- short-circuits the circulation and forces the heart to pump more blood overall to deliver the usual amount of blood to the vital organs.
• anaemia- requires the heart to pump more blood each minute to deliver enough oxygen to the tissues of the body.
• thyrotoxicosis- increases the body’s overall metabolism, thus increasing the demand for blood flow.